Fractures of the proximal femur are devastating events for individuals, particularly for the elderly for whom these type of injuries are frequent. In the United States alone there are more than 300,000 (Hudson et al. Clin Orthop: pp. 59-66, 1998) hip fractures and by the year 2050 the number is expected to double (Koval and Zuckerman, J. Am Acad Orthop Surg: 2(3) pp. 141-149, 1994; Montgomery and Lawson: Clin Orthop: pp. 62-68, 1978). AVN, also known as osteonecrosis, aseptic necrosis, ischemic bone necrosis, or osteochondritis dissecans, is an impairment of blood flow to bone tissues resulting in the subsequent death of the bone tissue and eventual fracture. AVN most commonly occurs in individuals between the ages of 30 and 60. Although it can occur in any bone, AVN most commonly affects the ends of long bones or the epiphysis, such as the femur. Other common sites are the humerus, knees, shoulders, and ankles. The disease can affect one or more bones at the same time or at different times. AVN can also be involved in other bones diseases, such as osteoarthritis.
Avascular necrosis of the bone or osteonecrosis has several causes. The loss of blood supply to the bone can be caused by traumatic or non-traumatic injuries, or increased pressure within the bone that causes the blood vessels to narrow and thus decreasing blood flow to bone tissues. During traumatic injuries, such as fractures or dislocations, the blood vessels can be damaged leading to comprised blood flow. This type of AVN may develop in more than 20% of the people with dislocated hip joints. The most common post-traumatic AVN are the femoral and humeral heads, the body of the talus, and the carpal scaphoid. Post-traumatic AVN arises because of impaired blood flow and is therefore dependent on the relative contributions of arterial blood flow to the femoral or humeral head and the extent of anastomoses for collateral blood flows.
In traumatic injuries, hip dislocations may tear the ligamentum teres and the joint capsule, hence compromising the blood vessels lying in the capsular reflections. Usually individuals with hips that remain dislocated for greater than 12 hours, 52% develop AVN. In individuals who's hip dislocations remain dislocated for less than 12 hours, usually 22% develop AVN. During postfracture fixation, the incidence of AVN ranges form 11 to 45% and does not seem to be related to the surgeon's skill or fixation device. Further, arthritic changes occurring in patients three or more years after a femoral neck fracture appear to be initiated by the collapse and fragmentation of small areas of AVN in or near the weight bearing region of the femoral head.
There are many other diseases or disorders that block the small blood vessels that supply the ends of long bones causing AVN. Non-traumatic causes include, but are not limited to, alcohol abuse, high doses of corticosteroids, especially when given for a prolonged period of time, diver's decompression sickness, sickle cell disease, Gaucher's disease, tumors, such as lymphomas, radiation therapy, and certain blood clotting disorders. However, in about 25% of people with AVN the cause is unknown. There are two major theories for the mechanism of action in the development of AVN in non-traumatic causes, intra- and extraluminal obliteration of the end blood vessels. Intraluminal obliteration can be caused for example, by fat emboli, sickle cells, or nitrogen bubbles during a diver's decompression sickness. Extraluminal obliteration can be caused for example, by increased bone marrow pressure due to Guacher cell proliferation or increased marrow fat. In addition there is also an idiopathic AVN. According to the American Academy of Orthopedic Surgeons, about 10,000 to 20,000 people develop osteonecrosis each year.
To determine the appropriate treatment for AVN the conditions must first be identified. However, in many patients AVN is often painless, at least in the beginning of the disorder. In fact, in the early stages patients may be asymptomatic and only as the disease progresses will patients experience joint pain. At first the pain emerges during weight bearing on the affected joint and later the pain remains even at rest. As AVN progresses the bone and surrounding joint surface may collapse and pain will then dramatically increase. Pain may become severe enough to limit the range of motion in the affected joint. Further involvement may also lead to debilitating osteoarthritis. In addition to a complete physical exam and medical history one or more imaging techniques may be required to diagnose AVN. X-rays and computed tomography (three dimensional x-rays) are useful to detect certain AVN conditions, such as, as the presence of bone collapse or osteoarthritis. That is, advanced stages of the disorder.
Therefore, AVN is frequently not diagnosed in its early stages and the disease may progress to advanced stages thus leading to the collapse of the joint. When traumatic injuries cause AVN, the disorder cannot be detected microscopically for days to weeks and may not be detected on x-rays for months after the injury. Magnetic resonance imaging (MRI) is the test of choice to detect or diagnose early AVN.
Appropriate treatment for AVN is essential to prevent the deterioration of the joint, pain, limitation of movement and subsequent disabilities. For most AVN conditions treatment is an ongoing process, and the goal is to improve the patient's mobility of the affected joint, stop further bone damage and ensure bone and joint survival. Conservative treatments are limited to drugs to reduce blood lipids, reducing blood clotting, use of nonsteroidal anti-inflammatory drugs (NSAIDs), reduced weight bearing, range of motion exercises, or electrical stimulation to induce bone growth. However, most AVN patients will eventually need surgery.
The simplest surgical procedure is core decompression, which involves removing the inner layer of bone of the affected region, that is, cutting out a plug of bone from the internal section of the bone to reduce the internal pressure. This permits an increase in blood flow to the area and allows blood vessel formation. This procedure appears to work best in individuals in the earliest stages of AVN, before progression to bone collapse and can reduce pain and slow progression of bone and joint destruction.
Another procedure is osteotomy, and this procedure involves reshaping the bone to reduce stress on the affected area. This practice is usually effective in individuals with advanced AVN and with a large area of affected bone. Recovery is lengthy and the patient's activities are very limited for 3 to 12 months. Another procedure is the use of bone grafting. This method can also be used after a core decompression procedure. The practice is to transplant healthy bone from another part of the patient's body to the AVN affected area. Commonly the bone grafts include vascular tissues, that is, include both artery and veins to increase and maintain blood supply to the AVN affected area. This method is complex and its effectiveness is not yet proven and the recovery period is usually 6-12 months. To be successful the body has to form not only new bone but also a new blood supply.
For people who are not good candidates for the procedures, arthroplasty or total joint replacement may be necessary. This is the only effective treatment in late stage AVN, when the joint is destroyed or when AVN has caused significant osteoarthritis on the other side of the joint. However, artificial joints do not last forever and in young people they may require replacement one or more times during the individual's lifetime. Various types of joint replacements are available, including a femoral head resurfacing process, and using a metal cap over the femoral head if the socket of the hip joint is not involved.
AVN has also been increasingly associated with the human immunodeficiency virus (HIV) disease, often with bilateral hip involvement. Whether, these individuals have the established risks factors or are at an increased risk due to the disease or its antiretroviral therapy requires further epidemiological studies.
An advantageous treatment result for a patient with AVN would be an increase blood flow to the affected area and hence new bone formation. New bone formation is accomplished by one or more mechanisms such as osteogenesis, osteoconduction and osteoinduction. However, for bone growth an adequate blood supply is required.
A system and method of treating osteonecrosis is described in U.S. Pat. No. 6,827,720 (the '720 patent). The '720 patent describes a technique of drilling channels in bone and inserting growth factors followed by a plug (not containing BMP) which compresses the growth factors. The channel is sealed with a plug or screw which is advanced into each channel and compacts the bone growth inducing compound. The bone growth compound is therefore biased toward the distal end of the channel. The compacting event forces the compound into the necrotic section of bone and the pressure causes the distal bone-voids to be filled with bone growth material. The plug or screw reinforces the subchondral bone and adds structural strength to the necrotic bone preventing collapse of the bone.
The present invention does not use a plug or screw to compact the bone growth factor implant. Further, screws are not required for structural stability, the implant is not biased toward the distal end of a channel, and tapping threads in the channel are also not required to advance a screw and compact the implant. In addition, the biological site identified for the angiogenesis implant does not require maintained structural support until new bone and vasculature develop (as described in the '720 patent). In the present invention, the implant provides angiogenesis in the identified site throughout the implant site and not just in the distal end of a channel. The entire procedure is less invasive and the implant is biocompatible and biodegradable and without the potential problem of future operations to remove screws or add additional compound in the channel left behind.